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The role of NOX in counterbalancing •NO activity was recently confirmed in patients with chronic granulomatous disease in which NOX genetic deficiency determined complete suppression of platelet O•2- production and increased levels of •NO [116]
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The Fe-S cofactor was shown to be bridged between two monomers via the N-terminal active site cysteine residues and two non-covalently bound GSH molecules [68]
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